Transcript Type of Steroids Used for systemic conditions in NTG and Control

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Steroid
Ever
Proportion of
Steroid Users
Proportion of Steroid Users in NTG
and Control Groups - Excluding Ant
seg surgery
0.35
0.3
0.25
0.2
0.15
0.1
0.05
0
*
*
*
NTG
Control
Steroid
Ever
Steroid Steroid
Before After 7/97
7/97
• The demographic and clinical characteristics of NTG and Control
groups is described in Table 1.
Table 1: Demographic and Clinical Characteristics of NTG and Control groups.
Age
(meansd)
Female
Race
White
Black
Hispanic
Other
HTN
DM
IOP Max
NTG
691.2
66%
55%
30%
7%
8%
41%
24%
18.40.27
Control
651.2
62%
p-value
P=0.01

65%


21%

5%

6%
44%

19%

17.30.29
P=0.0053
 indicates p>0.05
Fig 6: Type of Steroids Used for systemic
conditions in NTG and Control groups.
Fig 6: Type of Steroids Used for systemic
conditions in NTG and Control groups.
• Cataract extraction was significantly higher in the Control group
compared to the NTG group. No difference was found in any systemic
conditions between cases and controls. Fig. 4 and 5 show the
breakdown of conditions requiring steroids in the NTG and Control
group for systemic and ant. seg. ocular surgery respectively. Table 2
shows the conditions/procedures included in the Allergic, Inflammatory
and Total Ant. Seg. surgery categories. * indicates a statistically
significant difference between the NTG and control groups using 2.
Fig 4: Breakdown of systemic conditions
requiring steroids for NTG and Control
groups.
Proportion of People with Conditions
Requiring Steroid Use
Inflammatory
Sarcoid
Crohn’s disease
Graves disease
Polymyalgia Rheumatica
Systemic Lupus Erythematosis
Unspecified granulomatous disease
Ant. Seg. Surgeries
*Cataract Extration (CE)
Trabeculectomy
CE with Trab
• Fig. 6 shows the proportion of different types of steroids used for
systemic conditions by patients in the NTG and Control groups
respectively. Table 3 indicates the specific steroids included in the
Inhaler, Topical and Oral categories.
Fig 6: Type of Steroids Used for systemic
conditions in NTG and Control groups.
NTG
Table 3: Specific steroids included in the Inhaler,
Topical and Oral categories.
Control
Discussion
Proportion of People with Ant. Seg.
Surgery Requiring Steroid Use
0.3
0.2
0.25
0.2
NTG
Control
0.15
0.1
0.15
*
NTG
Control
0.1
0.05
0
Conclusions
• Univariate logistic regression analysis demonstrates a reduced odds
of NTG in steroid users.
• Controlling for age strengthens this association. Controlling by
indication for steroid use produces a result that is not statistically
significant.
• Larger numbers of cases and controls will be necessary to
demonstrate the true relation between steroid use and NTG.
References
Fig 5: Breakdown of Ant. Seg. surgeries requiring
steroids for NTG and Control groups.
0.35
0.05
ta
l
Results
Allergic
Allergic Rhinitis
Atopic Dermatitis
Eczema
Hayfever
• The speculation that steroids may prevent apoptosis is plausible
based on their ability to inhibit cell membrane lysis mediated by
phospholipases and oxidative enzymes. In our study, univariate
analysis suggests that steroid use was associated with a reduced
odds of having NTG.
• Problems regarding confounding by indication make the univariate
result of this study controversial. Larger scale prevalence studies
confirming our univariate finding are necessary. In these studies, very
careful estimate of steroid exposure would be indicated.
• Steroid exposure was defined as a dichotomous variable in three
ways relative to July 1, 1997 (1 year prior to the onset of the study).
 Steroid use for a period of 1 month at any given time in the past.
 Steroid use prior to July 1, 1997 for at least 1 month.
 Steroid use after July 1, 1997 for at least 1 month.
• The Odds ratio for steroid use was calculated using logistic regression
analysis for each definition of steroid use. The results were adjusted
for age, race, gender, hypertension, diabetes and diseases that were
indications for steroid use.
Table 2: Conditions/Procedures Included in the Allergic, Inflammatory and Ant Seg surg Categories.
Steroid Steroid
Before After 7/97
7/97
• Logistic regression predicted the Odd’s ratio to be 0.517 Model A
(p=0.07), 0.408 Model B (p=0.02), and 0.81 Model C (p>0.05) for the
development of NTG. The Odd’s ratios are plotted in Fig. 3 for the 3
Models. Models A, B, and C are described in Table 2.
To
Definition of Controls
• No evidence of glaucomatous optic neuropathy:
 cup/disc ratios < 0.6 OU
 cup/disc asymmetry < 0.2
 unremarkable red-free ophthalmoscopic examinations.
• No family history of glaucoma.
• Maximum IOP less then 21mmHg.
Controls did not undergo visual field testing.
Control
m
at
or
y
•
*
NTG
itis
•
*
la
m
•
•
•
Definition of NTG Cases
Patients with ONH or NFL appearance consistent with glaucoma.
Maximum IOP less then 21mmHg.
At least two reliable visual field examinations with reproducible
defects consistent with the nerve fiber layer pathology.
No evidence of exfoliation or trauma on slit lamp examination and no
evidence of an occludable angle or angle recession on gonioscopy.
Patients with pre-existing iridotomies were excluded form the study.
*
In
f
The sample consisted of 154 patients:
• 72 NTG (mean age 69.0  10; 44-85; 25M, 47F)
• 82 controls (mean age 64.8  11; 44-86; 31M, 51F)
0.35
0.3
0.25
0.2
0.15
0.1
0.05
0
Ar
th
r
Sample
Fig 2: Steroid Use excluding ocular surgery in
NTG and Control groups
Proportion of Steroid Users in NTG
and Control Groups
rg
ic
• To study the association of steroid use and prevalence of NTG in a
clinic-based population.
• Ophthalmic information regarding ocular conditions, surgeries and
maximum IOP was corroborated from the patient’s eye records.
• Non-ophthalmic information was confirmed by a review of the patient’s
electronic medical record. These records contained information
regarding the patient’s medical conditions, as well as the date of first
and filled prescription for all medications.
Fig 1: Steroid Use in NTG and Control groups
Al
le
Purpose
• The sample was selected from patients aged 40 and older who
presented to the Division of Ophthalmology at Brigham and Women’s
Hospital from July 1998 to January 1999. Patients were required to
have electronic medical records dating back to at least 1996.
• All patients were examined by a single observer.
• Each patient was questioned about their past ocular, medical and
surgical history, as well as current use of medications. An extensive
history of past and present steroid use was obtained which included
name of the steroid, dose, frequency of administration, duration, and
time period of use.
• Subsequently, all patients underwent a complete eye examination.
• Any patient suspected of having glaucomatous optic neuropathy
based on the appearance of the optic nerve and nerve fiber layer
underwent visual field testing with either the Humphrey or Goldmann
perimeters. Patients with unreliable visual fields or no reproducible
visual field loss were excluded.
Results - con’t
• The NTG group used significantly less steroids then the control group
for all definitions of steroid exposure. Fig. 1 and 2 show the proportion
of people taking steroids in the NTG and Control group for total steroid
use and steroid use excluding anterior segment surgery respectively.
* indicates a statistically significant difference between the NTG and
Control groups using 2.
O
PD
Finally there is data suggesting an immune deviation in patients with
NTG2 where serum antibodies directed to retinal elements have been
found. Exogenous steroids could prevent NTG by nonspecifically
blunting this aberrant response.
Results - con’t
C
Steroids are known to be nonspecific blockers of cell membrane
lipases6 which may inhibit apoptosis in this setting. Furthermore,
certain glucocorticoids are thought to intercalate into the cell membrane
and decrease neuronal and vascular membrane fluidity by inhibiting
oxygen free radical-induced lipid peroxidation7. Studies have shown
that RGC survival in vitro is dependent on the addition of steroids to the
culture8.
Methods
Proprotion of Steroid
Users
Retinal ganglion cells (RGC) die by apoptosis in both high tension1 and
low tension2 glaucoma. Ischemia and neuronal compression may
deprive the RGCs of essential trophic factors necessary for their
survival3. When apoptosis occurs, the RGC cytoplasmic volume
decreases and the cell membrane ruptures, while the nucleus
condenses4. RGC membrane lysis is mediated by phospholipases and
oxidative enzymes. Leaky RGC may release other toxic substances
such as excitatory amino acids, which further damages neighboring
cells3. Glutamate, an excitatory amino acid, has been found in elevated
concentrations in the vitreous body of glaucomatous eyes5.
England College of Optometry, Boston, MA
th
m
a
Introduction
and Womens Hospital,
2New
M.
2
Jacisin
As
1Brigham
T.
1
Farra ,
0
CE
Total
1 Quigley HA, Nickells RW, Kerrigan LA, Pease ME, Thibault DJ, Zack DJ. Retinal ganglion cell death in
experimental glaucoma and after axotomy occurs by apoptosis. Invest Ophthalmol Vis Sci 1995;36:77486.
2 Wax MB, Tezel G, Edward PD. Clinical and ocular histopathological findings in a patient with normalpressure glaucoma. Arch Ophthalmol 1998; 116:993-1001.
3 Chew SJ, Ritch R. Neuroprotection: the next breakthrough in glaucoma? Proceedings of the Third
Annual Optic Nerve Rescue and Restoration Think Tank. J Glaucoma 1997; 6:263-6.
4 Spaeth GL. Glaucoma, apoptosis, death, and life. Acta Ophthalmol Scand Suppl 1998; 227:9-15.
5 Dreyer EB, Zurakowski D, Schumer RA, Podos SM, Lipton SA. Elevated glutamate levels in the vitreous
body of humans and monkeys with glaucoma. Arch Ophthalmol 1996; 114:299-305.
6 Lee HM, Weinstein JN, Meller ST, Hayashi N, Spratt KF, Gebhart GF. The role of steroids and their effects
on phospholipase A2 in an animal model of radiculopathy. Spine 1998; 23(11):1191-6.
7 Hall ED. Neuroprotective actions of glucocorticoid and nonglucocorticoid steroids in acute neuronal
injury. Cell Mol Neurobiol 1993; 13:415-32.
8 Lindsey JD, Weinreb RN. Survival and differentiation of purified retinal ganglion cells in a chemically
defined microenvironment. Invest Ophthalmol Vis Sci 1994; 35:3640-8.45